In vivo assessment of pulmonary vascular integrity in experimental pulmonary edema

across the lungs ["C]urea remains in the vascular com-partment, but its molecular size and solubility suggest it might escape abnormally permeable vessels. To test the hypothesis that ["C]urea might be used to dis-tinguish pulmonary edema due to acutely increased in-travascular pressure from that due to vascular damage by alloxan, we studied [5tCr]erythrocytes (r), ['I]albu-min (a), ["C]urea (u), and tritiated water as dilution indicators in the pulmonary circulation of anesthetized dogs. In addition, the adequacy of albumin as an intra-vascular indicator was evaluated. Indicator curves, blood gases, hematocrit, and vas-cular pressures were determined during a base-line period and repeated 30 and 60 min after treatment in five groups of dogs: (a) saline control, (b) alloxan edema, (c) epinephrine infusion, (d) volume overload, and (e) left atrial (LA) balloon obstruction. Groups b, d, and e developed a similar degree of edema judging by wet/dry lung weights and histology. Groups a and c did not develop edema. In alloxan edema, differences between the mean transit time vol-ume of u and r (V.-.) increased over base line at 30 (P < 0.01) and 60 min (P < 0.02); the differences between the mean transit time volume of a and r (V.-,) increased slightly at 30 (P < 0.03) and 60 min (